A number of developmental disorders are associated with cortical injury that occurs during the period of neuronal migration to the cortex and leads to areas of focal microgyria and molecular layer glio-neuronal heterotopias. These anomalies have been reported in the brains of individuals with developmental dyslexia and have been modeled in the rodent for the purpose of understanding the link between anatomical and behavioral changes. In many dyslexics and other developmentally language impaired individuals, the anatomical anomalies are associated with problems with low level auditory processing. When microgyria are experimentally induced in rats, difficulties performing some learning tasks and in discriminating rapid sound changes are seen that are similar to those in language impaired individuals appear. These results, thus, indicate a causal relationship between cortical anomaly induction and temporal and other processing deficits. Anatomical studies in the rodent show that cortico-cortical and cortico-thalamic connectivity is altered by microgyria induction, as well as cellular changes in abnormal and adjacent cortex and thalamus. This Program Project aims to deepen and broaden our knowledge of anatomical-physiological-behavioral mechanisms in the rodent model of temporal processing deficits. This component of the Program Project grant is designed to explore, at the systems neurophysiological level, the neural bases for the specific auditory temporal processing deficits associated with cortical microgyria. Abnormal cortical electric field responses to acoustic modulations are seen in microgyria, which has led us to the hypothesis that microgyria causes temporal processing deficits in the auditory cortex. We propose to use white noise acoustic stimuli for recording and analyzing cortical and subcortical brain evoked potentials in microgyria animals. These analytic tools are much more powerful than those traditionally employed for human evoked potentials studies and will allow us to characterize specific spectral and temporal processing deficits. Next, we propose to extensively map spectral-temporal features encoding in single neurons of the primary auditory cortex, with the prediction that microgyria animals will show altered features encoding in auditory cortex. Finally, we propose to show that the cellular changes in auditory thalamus associated with dyslexia and microgyria are associated with altered organization of layer VI cortico-cortical connections and thalamo-cortical connections. Identifying details of auditory cortical organizations and specific spectral and temporal processing associated with microgyria in early development should lead to strategies for improved diagnosis and treatment.